TY  - JOUR
  - Wang, J. D.,Fan, X. J.,Lindholm, C.,Bennett, M.,O'Connoll, J.,Shanahan, F.,Brooks, E. G.,Reyes, V. E.,Ernst, P. B.
  - 2000
  - July
  - Infection and Immunity
  - Helicobacter pylori modulates lymphoepithelial cell interactions leading to epithelial cell damage through Fas/Fas ligand interactions
  - Validated
  - ()
  - 68
  - 7
  - 4303
  - 4311
  - Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Pas receptor expression was detected on freshly isolated gastric epithelial tells by dow cytometry and immunohistochemistry, and this level of expression was increased during infection with H, pylori. The expression of Pas receptor on three gastric epithelial cell lines was increased by N, pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after crosslinking of Pas with specific antibodies. Fast expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express Fast, as evidenced by reverse transcription-PCR and killing of target cells expressing Pas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Pas receptor and Fast inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Pas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions.Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Pas receptor expression was detected on freshly isolated gastric epithelial tells by dow cytometry and immunohistochemistry, and this level of expression was increased during infection with H, pylori. The expression of Pas receptor on three gastric epithelial cell lines was increased by N, pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after crosslinking of Pas with specific antibodies. Fast expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express Fast, as evidenced by reverse transcription-PCR and killing of target cells expressing Pas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Pas receptor and Fast inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Pas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions.
  - 0019-95670019-9567
  - ://WOS:000087710200064://WOS:000087710200064
DA  - 2000/07
ER  - 

@article{V235379696,
   = {Wang,  J. D. and Fan,  X. J. and Lindholm,  C. and Bennett,  M. and O'Connoll,  J. and Shanahan,  F. and Brooks,  E. G. and Reyes,  V. E. and Ernst,  P. B. },
   = {2000},
   = {July},
   = {Infection and Immunity},
   = {Helicobacter pylori modulates lymphoepithelial cell interactions leading to epithelial cell damage through Fas/Fas ligand interactions},
   = {Validated},
   = {()},
   = {68},
   = {7},
  pages = {4303--4311},
   = {{Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Pas receptor expression was detected on freshly isolated gastric epithelial tells by dow cytometry and immunohistochemistry, and this level of expression was increased during infection with H, pylori. The expression of Pas receptor on three gastric epithelial cell lines was increased by N, pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after crosslinking of Pas with specific antibodies. Fast expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express Fast, as evidenced by reverse transcription-PCR and killing of target cells expressing Pas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Pas receptor and Fast inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Pas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions.Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Pas receptor expression was detected on freshly isolated gastric epithelial tells by dow cytometry and immunohistochemistry, and this level of expression was increased during infection with H, pylori. The expression of Pas receptor on three gastric epithelial cell lines was increased by N, pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after crosslinking of Pas with specific antibodies. Fast expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express Fast, as evidenced by reverse transcription-PCR and killing of target cells expressing Pas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Pas receptor and Fast inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Pas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions.}},
  issn = {0019-95670019-9567},
   = {://WOS:000087710200064://WOS:000087710200064},
  source = {IRIS}
}